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Oral squamous carcinoma cells stimulated by Porphyromonas gingivalis-derived lipopolysaccharide induce osteoclastogenesis through a paracrine mechanism

  • Bo Ram Keum (Department of Oral Physiology, School of Dentistry, Pusan National University) ;
  • Soon Chul Heo (Department of Oral Physiology, School of Dentistry, Pusan National University) ;
  • Hyung Joon Kim (Department of Oral Physiology, School of Dentistry, Pusan National University)
  • Received : 2024.07.11
  • Accepted : 2024.07.26
  • Published : 2024.09.30

Abstract

Periodontal disease (PD) is strongly linked to increased risk of oral squamous cell carcinoma (OSCC); however, the specific mechanism through which the development of PD and OSCC is simultaneously promoted remains unclear. This study explored the impact of periodontal pathogens on OSCC progression and the contribution of periodontal pathogen-stimulated OSCC to PD development. The expression of osteoclastogenesis-inducing factors was assessed using quantitative reverse transcription polymerase chain reaction analysis following stimulation of OSCC with lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis (Pg), a pathogen commonly responsible for PD. The cell counting kit-8 assay was used to determine the effects of Pg-LPS on OSCC proliferation and drug resistance to cisplatin and 5-fluorouracil. The effects of conditioned medium (CM) derived from Pg-LPS-stimulated OSCC on osteoclastogenesis was evaluated using tartrate-resistant acid phosphatase (TRAP) staining on bone marrow-derived macrophages (BMMs). Pg-LPS administration in SCC-25 and YD-8 OSCC cell lines induced a significant increase in receptor activator of nuclear factor kappa-B ligand mRNA expression; however, it did not affect cell proliferation. Treatment with CM derived from Pg-LPS-stimulated SCC-25 or YD-8 cells markedly enhanced the formation of TRAP-positive multinucleated cells during osteoclast differentiation of BMMs. Altogether, these findings demonstrate that Pg-LPS-stimulated OSCC promoted osteoclastogenesis through a paracrine mechanism.

Keywords

Acknowledgement

이 과제는 부산대학교 기본연구지원사업(2년)에 의하여 연구되었음.

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